The purpose of this project is to study the mechanism of gallium-67 accumulation in inflammatory lesions. We have demonstrated that gallium-67 is taken up by human polymorphonuclear leukocytes (PMN) and a variety of microorganisms. We have also demonstrated that neither PMN nor bacteria are essential, when using an animal model, for the accumulation of gallium at the site of inflammation and that most of the gallium present in inflammatory lesions is in the non-cellular fraction (2,500 g supernate). Furthermore, increased capillary permeability seems to play an important role in gallium accumulation. We propose to extend our observation and study (1) the effect of unsaturated iron-binding capacity on the organ distribution and abscess accumulation of gallium, (2) determine the degree of protein-binding and (3) identify the protein(s) which binds gallium in the 2,500 g supernate of the inflammatory exudate.